RESUMO
BACKGROUND: Mobile ultraviolet (UV) disinfection uses UV-C light to render microorganisms nonviable and reduce environmental transmission of pathogens in hospital settings. Optimal strategies for deployment must consider the cost, physical layout, and staffing resources. The aim of this quality improvement study was to increase UV disinfection utilization by developing novel deployment strategies without adding resources. METHODS: A novel deployment strategy and tools were developed by a multidisciplinary group that included infection prevention, environmental services, and nursing unit staff. Utilization was tracked via a manufacturer-supported database. The infection prevention team analyzed the weekly UV disinfection minutes, cycles, and proportions of cycles completed in defined areas across 4 periods: baseline, pilot, baseline 2, and intervention. RESULTS: The median (range) disinfection cycle times per week during a geographically confined pilot (4,985 minutes [3,476-6,551] minutes) and the intervention period (1,454 [512-3,085] minutes) were lower than either baseline period (5,394 [3,953-6,987] and 6,641 [2,830-7,276] minutes, respectively). Cycles per week were lower in the intervention period than in the preceding 3 periods. CONCLUSIONS: Use of UV disinfection in acute care settings should be guided by multidisciplinary groups balancing resources against efficacy and using tailored tools to promote efficiency.
RESUMO
Candida albicans is the most common opportunistic fungal pathogen and causes local and systemic disease in immunocompromised patients. Alveolar macrophages (AMs) are pivotal for the clearance of C. albicans from the lung. Activated AMs secrete 5-lipoxygenase-derived leukotrienes (LTs), which in turn enhance phagocytosis and microbicidal activity against a diverse array of pathogens. Our aim was to investigate the role of LTB(4) and LTD(4) in AM antimicrobial functions against C. albicans and the signaling pathways involved. Pharmacologic and genetic inhibition of LT biosynthesis as well as receptor antagonism reduced phagocytosis of C. albicans when compared with untreated or WT controls. Conversely, exogenous LTs of both classes augmented base-line C. albicans phagocytosis by AMs. Although LTB(4) enhanced mainly mannose receptor-dependent fungal ingestion, LTD(4) enhanced mainly dectin-1 receptor-mediated phagocytosis. LT enhancement of yeast ingestion was dependent on protein kinase C-δ (PKCδ) and PI3K but not PKCα and MAPK activation. Both LTs reduced activation of cofilin-1, whereas they enhanced total cellular F-actin; however, LTB(4) accomplished this through the activation of LIM kinases (LIMKs) 1 and 2, whereas LTD(4) did so exclusively via LIMK-2. Finally, both exogenous LTB(4) and LTD(4) enhanced AM fungicidal activity in an NADPH oxidase-dependent manner. Our data identify LTB(4) and LTD(4) as key mediators of innate immunity against C. albicans, which act by both distinct and conserved signaling mechanisms to enhance multiple antimicrobial functions of AMs.